achilles tendinopathy tendinopathy.pdf · the name ‘achilles tendon’ is derived from the iliad...

Dr George KonidarisFoot & Ankle, Hip and Knee Surgery

Dr George Konidaris

www.orthosports.com.au

47‐49 Burwood Road, Concord 160 Belmore Road, Randwick

Achilles Tendinopathy

http://www.orthosports.com.au/


History

•

The name ‘Achilles Tendon’

is derived from the Iliad by Homer.

•

Achilles was made invulnerable by his Goddess mother Thetis, who plunged him into the river Styx, while holding him by one heel. This part was

not bathed and hence not protected.•

This heel was the site were he was mortally

wounded by a poisoned arrow launched from the bow of ‘Paris’

during the Trojan war.


Introduction

•

Previously known as “Achilles Tendinitis”•

Minimal acute inflammation

•

Better referred to as “Achilles Tendinopathy”

•

Clinical syndrome of Pain, Swelling and impaired performance in the Achilles

Tendon


Epidemiology and Incidence

•

Non‐I AT is most common in 30‐40s, M > F•

Seen in 7‐9% of top level mid‐long distance

runners •

Also seen in Soccer, track and field, tennis

•

In athletes with tendinopathy

–

66% have non‐insertional, 23% insertional

•

I AT is seen in an older less active populatio


Aetiology of Pain

•

Not yet completely determined•

Is it?–

intratendinous

degenerative changes

–

expansion of tendon from increased ground substance and GAG concentration

–

neovascularisation

•

Up to 34% of asymptomatic tendons had histopathological changes in one study

•

Ingrowth

of sensory/sympathetic nerves from paratenon plays a role.


Achilles Tendinopathy ‐ Histology

•

“Degenerative and Overuse condition with attempts of Repair”

•

Collagen degeneration, fibre disorganisation and thinning with hyalinisation and fibre separation

by increased ground substance (GAGs)•

Scattered vascular ingrowth

with areas of

necrosis and calcification•

Nerve ingrowth

occurs

•

Zone of hypovascularisation


Classification

•

Midportion

Achilles Tendinopathy•

Paratendinopathy–

Acute or Chronic

•

Insertional

Achilles Tendinopathy•

Retrocalcaneal

Bursitis

•

Superficial Calcaneal Bursitis

–

Others –Pudda

classification


Clinical

•

Initially ‐

Start up pain, at end of activity•

Progresses to during activity

•

Then interferes with ADLS, shoe wear problems•

Acutely can be swollen, erythematous

and tender

+‐

crepetations•

Chronically –

activity related pain, crepitations

and swelling decrease, with tender nodular swelling


Examination

•

Paratendinosis

Vs Tendinosis–

Arc test –

swelling in the tendon will move

with plantar/dorsi

flexion of the ankle–

Royal London Hospital test –

swelling that is

most painful becomes less tender withmaximal dorsiflexion

indicates tendinopathy

•

Insertional

Vs Non‐

insertional•

Calcaneal exostosis (Haglunds deformity)


Examination

•

Retrocalcaneal

bursitis–

Pinch test – pinch infront

of distal TA may

reproduce pain, and with dorsiflexion

may intensify the pain.

•

Sensitivity 50‐60%, Specificity 80‐90%•

Exclude –

posterior impingement

–

Acute ruptures


Imaging

•

XR–

Parallel pitch lines

•

Ultrasound–

User dependant

–

Colour doppler

can show areas of neo‐vascularisation

•

MRI


Treatment

•

Relieve symptoms initially–

Rest, cross train, ice, shoe modifications,

simple analgesia, heel raise/brace (AirHeel)–

NSAIDS (little evidence in chronic tendinosis)

–

Corticosteroids (controversial‐

risk of rupture small and little evidence to support it)

•

Better for peritendinopathy/retrocalcaneal

bursitis

–

Correct training errors–

MLA orthotics in hyperpronators


Treatment

•

Eccentric stretch and strength program–

Less effective in insertional

AT

•

Transcutaneous

Glyceryl

Trinitrate (GTN)–

Some evidence to support its use (Paoloni

2007)–

Watch out for headaches


Treatment

•

Sclerosant

injections (Polidocanol)–

Destroys neovessels

and nerves

–

Small risk of rupture

•

Volume injections (Brisement)–

High volume saline/LA/hydrocortisone

–

Destroys neovessels

and ?nerves, releases adhesions

–

Some evidence to support its use (Chan 2008)–

Better for peritendinosis


Treatment

•

Prolotherapy–

Hyperosmolar

dextrose and LA peritendinous

injection, creates an inflammatory response–

No good supportive evidence

•

Shock‐wave therapy–

May be more beneficial in insertional/calcific

–

Comparable results have been seen to eccentric loading (Rompe

2007 AmJSM)


Treatment

•

PRP injections–

No evidence to justify its use (De Vos

2010

JAMA)–

He compared eccentric program with either

saline or PRP injections


Treatment

•

Low‐level laser therapy–

Insufficient evidence to support it use


Treatment ‐ Surgical

•

Usually involve removal of inflamed or diseased tissue and decompression of mechanical pressure from adjacent

calcaneus

+‐

tendon transfer•

Complication rate up to 11%–

Mainly wound healing

–

Therefore skin and vascular compromise are contraindications



•

Percutaneous

longitudinal tenotomies–

Better for non‐insertional

•

Achilles Tendonscopy

with release of adhesions, tendon debridement

•

Plantaris

excision +‐

ventral Achilles tendon scraping

•

Calcaneoplasty

(Haglunds

deformity debridement)

–

Open or endoscopic



•

FHL muscle belly transfer–

Used in non‐insertional

tendinopathy

–

?bring blood supply to tendon

•

FHL tendon transfer–

If more than 50% of tendon debrided

–

Patients notice Hallux weakness, esp

when bearfooted

•

Other options include FDL and Plantaris



•

Reconstruction–

Debridement with a large gap remaining

–

Options include•

Primary repair (less than 3cm)

•

V‐Y lengthening or Turndown flap (3‐6 cm)•

Tendon transfer (usually FHL) (when > 6cm)


•

Thank you

achilles tendinopathy tendinopathy.pdf · the name ‘achilles tendon’ is derived from the iliad...

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